International Journal of Medical Laboratory
Volume:10 Issue: 1, Feb 2023

Limited information is available on the frequency of advanced adenomas in diminutive colon polyps. Thus, this study aimed to investigate the pathological characteristics and the frequency of high-grade dysplasia in diminutive colorectal polyps in individuals referred to colonoscopy examination in Kermanshah, Iran.

Demographics characteristics, location and diameter of the polyp, histological assessment of the polyps, grade, and others were retrieved from colonoscopy reports.

During the study period, 250 diminutive colorectal polyps were detected. The histological assessment showed that 36.4% were adenomatous, 32.8% were hyperplastic, and 30.8% were inflammatory polyps. Only two diminutive polyps (0.8%) had high-grade dysplasia, and the frequency of adenocarcinoma in our study was 0.4%. Besides, the frequency of adenomatous polyps was higher in the proximal versus the distal colon. These findings emphasize the urgent need for a colorectal cancer screening plan in the Iranian population to improve therapeutic outcomes.

Neutrophils are innate immune system phagocytes that play a central role in immunity defense. They are equipped with effective antimicrobial that is mainly stored in specialized granules. Considering that, it can also damage host tissue. Neutrophil deployment is heavily regulated through various strategies, including phagocytosis, reactive oxygen species, production degranulation, and the formation of neutrophil extracellular traps (NET). This review article will discuss its role in inflammatory, autoimmune diseases, and cancer and place it as a therapeutic target. It depicts that NET formation includes a suicide program morphologically different from other types of cell death, such as apoptosis and necrosis. Besides, NETs have unique DNA and antimicrobial peptide structures, and antimicrobial activity is among the functions of neutrophils as the first response to inflammation. So, it plays a pivotal role in the pathophysiology of various diseases, especially inflammatory and autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. As a result, it can be effective in the pathogenesis of many diseases, and its pathogenic role can be used as a therapeutic target.

Hospital infections and their antibiotic resistance have become a global concern recently. One of the most prominent factors in hospital infections is Pseudomonas aeruginosa (P. aeruginosa), which can become resistant to many antibiotics due to its ability to form biofilms. Recently, scientists have tried to replace antibiotic therapy with alternative therapies such as probiotics which can reduce or eliminate the pathogenic bacteria's ability to form biofilms. Therefore, the present study revealed that some genes, such as algD
and PpyR, were involved in biofilm formation in P. aeruginosa. Furthermore, the inhibitory effect of the supernatant of lactobacillus agilis on the biofilm formation of P. aeruginosa was evaluated in the current study.

In this study, the effect of the supernatant of probiotic Lactobacillus agilis on the biofilm formation of P. aeruginosa and also the expression of two genes effective in biofilm formation (algD and PpyR) were investigated. Antibiograms were performed to detect the most resistant bacteria since there is a link between biofilm formation and antibiotic resistance. Further, the effects of probiotics on the expression of PpyR and algD genes were discussed.

Results showed that the biofilm formation of P. aeruginosa was significantly reduced in the presence of lactobacillus agilis.

According to the current study, it could be concluded that because of antibiotics resistance and their associated mechanisms, probiotics could be used as a replacement for antibiotics in many treatments.

Colorectal cancer (CRC) is one of the most common human cancers. Currently, carcinoembryonic antigen (CEA) is used as the main standard biomarker of CRC, though this biomarker is not specifically made for CRC and, in a minority of cases, shows inadequate sensitivity. Therefore, searching for novel accessory biomarkers may fill these gaps in clinical management. miRNAs physiologically regulate various metabolic processes and are misregulated in various cancers. Therefore, the present investigation was conducted to evaluate miR-1 levels in CRC samples.

The CRC and adjacent tissue samples were obtained from 24 patients. In addition, sera were collected from the patient group and 24 healthy controls. Total RNA was extracted from tissue samples, and cDNA was synthesized. Real-time PCR determined the expression of miR-1. Serum levels of CEA were also measured using a Monobind ELISA assay kit.

The level of miR-1 in CRC tumors was significantly down-regulated. Moreover, patients with metastasis showed lower expression of miR-1 compared to cases without metastasis; however, this difference was not statistically significant. The ROC curve for miR-1 showed an AUC of 0.69. In addition, ROC analysis revealed a sensitivity of 70.27% and a specificity of 62.96% for miR-1.

There is still a need for new upcoming markers in addition to the main CRC biomarker, CEA. The levels of miR-1 in colorectal cancer tissue samples may provide additional information for the management and follow-up of CRC patients; though, the clinical application needs further studies.

The occurrence of single and double-strand breaks of DNA damage is the major obstacle for proliferation under various environmental factors and, if not repaired, can result in many consequences, including mutation, cell death, and others. So, the present study was conducted to evaluate the damage of DNA and the expression status of DNA repair system genes before and after stem cell proliferation.

The MACS method isolated the umbilical cord blood hematopoietic stem cells (UCB-HSCs). In order to investigate cell death, the study of Annexin V/PI was done by flow cytometry. Comet assay made observation and identification of DNA breaks, and the expression of genes normally involved in the repair of DNA breaks was evaluated by real-time polymerase chain reaction.

The average number of stem cells increased by 1.9-fold after three days of proliferation. The apoptotic percentage of cells was negligible (less than 0.2%), and the purity of the CD34+ cells was reduced by about one-third in three days (67%). By examining the expression of DNA repair genes, including KU70, KU80, RAD51, and XRCC1, their increased fold change was not significant. In a microscopic examination of stem cells in the comet assay, there was no significant difference between DNA damage before (1.33% ± 0.31) and after (2.08% ± 0.92) replication.

In our investigation, neither DNA damage nor changes in the DNA break repair were observed. However, further studies are required to clarify the DNA break repair by recruiting more UCB-HSCs samples.

β-thalassemia is the most common genetic disorder worldwide. β-thalassemia major results in severe anemia and serious complications. So, this study aims to evaluate the hematological and biochemical markers in β-thalassemia major patients in Bushehr city.

Our study included 94 transfusion-dependent β-thalassemia major were compared with 94 normal healthy subjects as controls. Hematological assessments included complete blood count indices. The biochemical evaluations included liver, kidney, and thyroid function tests, lipid profile, sodium, potassium, calcium, phosphorus, fasting blood sugar, and serum ferritin.

All hematological parameters in patients, such as hemoglobin (p < 0.01), hematocrit (p < 0.01), mean corpuscular volume (p < 0.05), and mean corpuscular hemoglobin (p <0.05), were significantly reduced compared to the control group except mean corpuscular hemoglobin concentration which was insignificant (p > 0.05). Higher levels of triglyceride, phosphorus, fasting blood sugar, aspartate aminotransferase, alanine transaminase, alkaline phosphatase, uric acid, total and direct bilirubin, and lower levels of cholesterol, high-density lipoprotein, and low-density lipoprotein were observed in patients in comparison to the control group (p < 0.05). Serum sodium, potassium, calcium, and albumin was not significantly different from the control group (p > 0.05). The prevalence of primary hypothyroidism (thyroid stimulating hormone > 4.5 mIU/l and T4 < 5.6 μg/dl) was reported at 5.31%.

This study emphasized the necessity for regular follow-up and evaluation of β-thalassemia, which could be used to improve treatment protocols.

A monoclonal antibody (mAb) can unambiguously identify, quantify, and purify an antigen or particular epitope at a large scale. The superiority of these antibodies lies in their specificity for the antigenic determinant. So, this study aims to prepare mouse mAb-secreting hybridoma against human gamma interferon (IFN-γ) and determine the produced antibody's characters.

Mouse splenic B lymphocytes immunized with recombinant human IFN-γ were fused with mouse SP2/0 cells. The hybridized cells were selected by hypoxanthine-aminopterin-thymidine and hypoxanthine-thymidine media to obtain monoclonal antibody-producing hybridoma cells. Finally, indirect enzyme-linked immunosorbent assay (ELISA), sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and western blot were used to confirm the creation of antibody-secreting hybridoma cells.

mAb against IFN-γ were produced by fusing SP2/0 mouse non-secretory myeloma cell line with the spleen cells of immunized mice. This antibody's indirect ELISA optical density was 2.055 on average, and the desired antibody bands were confirmed in SDS-PAGE compared to Septicol® (commercial antibody). Also, in the western blot, the desired antibody could bind to the antigen. IFN-γ transferred on nitrocellulose membrane. In ELISA and western blot tests, anti-mouse IgG conjugated antibodies were used; therefore, the mAb IgG isotype was taken into consideration.

 In this study, a mouse mAb was obtained by immunization of Balb/C mice and fusion of spleen cells of these mice with the SP2/0 cells, which can specifically bind to recombinant human IFN-γ and can be used to detect IFN-γ secretion in all types of intracellular infections, including latent tuberculosis.

The concomitant use of antioxidants during chemotherapy is controversial. It is unknown whether antioxidants increase or decrease the effectiveness of anticancer drugs. Therefore, the present study aimed to investigate ubiquinone's cytotoxic and antioxidant effects on the HepG2 cell line.

The HepG2 cell line was chosen as an experimental model for hepatocellular carcinoma in this study. The cytotoxic effect of ubiquinone was assessed as a function of time and concentration using the colorimetric MTT assay. The half-maximal inhibitory concentration (IC50) was determined to assess the cytotoxic effects of different ubiquinone concentrations. The protective impacts of ubiquinone on HepG2 cells were evaluated by assessing the oxidative stress profile.

The MTT showed that the IC50 after treatment with ubiquinone was 350 and 335 μM at 24 and 48 hours, respectively. Evaluation of redox homeostasis in HepG2 cells using three doses of ubiquinone, including IC50 and one dose higher and one dose lower than IC50, showed a decrease in oxidative stress and an increase in the antioxidant capacity of HepG2 cells in a dose-dependent manner (p < 0.01). An increase in redox hemostasis decreased the viability of HepG2 cells.

Our results showed ubiquinone could reduce cancer cell survival by interfering in redox oxidative-redox status. Therefore, ubiquinone can be used as an antioxidant supplement along with chemotherapy drugs.